Learning Objectives. How big is the problem? ACUTE KIDNEY INJURY

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ACUTE KIDNEY INJURY Karen Innocent, DNP, RN, CRNP, ANP-BC, CMSRN Executive Director, Continuing Education Wolters Kluwer Health, Inc May 2016 Orlando FL Learning Objectives Identify the risk factors and causes of acute kidney injury. Identify the clinical definition and signs of acute kidney injury. Select appropriate interventions for prevention and management of acute kidney injury. How big is the problem? Most data is available from ICU patients 1% to 25% Incidence 15% to 60% Mortality Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int 2012; 2:1 138. 1

Why should we should be concerned? Outcomes of AKI Decreased life expectancy Readmissions Worsening chronic kidney disease Progression to end stage renal disease Higher health care costs Top 3 Causes of AKI 1. Decreased perfusion 2. Nephrotoxic drugs 3. Intravenous contrast dye Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int 2012; 2:1 138. 2

Decreased Kidney Perfusion Causes of Decreased Kidney Perfusion Myocardial Infarction Health failure Cardiovascular Surgery Cerebrovascular Accident Hypovolemia Trauma, blood loss Nephrotoxic Drugs 3

Nephrotoxity: Clinical Definition A decrease in renal function as evidenced by a rise in serum creatinine levels following the initiation of a drug signals the possibility of drug-induced renal injury. Drug-Induced Nephrotoxicity Cynthia A. Naughton. Am Fam Physician. 2008;78(6):743-750. Nephrotoxic agents that alter intraglomerular hemodynamics Angiotensin Converting Enzyme Inhibitors Angiotensin Receptor Blockers NSAIDs Transplant / Immunosuppressants: Cyclosporine or tacrolimus Nephrotoxic agents associated with tubular cell toxicity Amphotericin B Aminoglycosides: Gentamicin, vancomycin, tobramycin Contrast dye 4

Nephrotoxic drugs associated with chronic interstitial nephropathy Acetaminophen Aspirin NSAIDs Nephrotoxicity related to crystal nephropathy Acyclovir Methotrexate Sulfa antibiotics Triamterene Intravenous Contrast Dye 5

Contrast-induced AKI Risk Factors Older adult > 75 years 1, 2 Concurrent administration of nephrotoxic agents 1, 2 Preexisting / chronic kidney disease 1,2 Intra-Aortic Balloon Pump 1 Anemia 1 Diabetes mellitus 1, 2 Cirrhosis 2 Heart failure 1, 2 Other history of impaired renal perfusion 2 1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int 2012; 2:1 138. 2. Vandenberghe, W., De Corte, W., Hoste, E.A.J. (2014). Contrast-associated AKI in the critically ill: relevant or irrelevant?. Current Opinion in Critical Care: 20(6):596-605. Acute Kidney Diseases Acute Glomerulonephritis Nephritis Vasculitis Thrombotic microangiopathy Urinary Tract Obstruction What do rifles have to do with AKI? 6

OOPS! Not rifles R.I.F.L.E. Diagnosis and Staging Risk Injury Failure Loss End-Stage Renal Disease Definition of Acute Kidney Injury Increase in SCr by X0.3 mg/dl (X26.5 lmol/l) within 48 hours Increase in SCr to X1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; Urine volume <0.5 ml/kg/h for 6 hours. Normal Range = Creatinine: 0.8 to 1.4 mg/dl Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int 2012; 2:1 138. 7

Stages of AKI Stage 1 - Risk SCr increased x0.3 mg/dl or x26.5 mmol/l from baseline Urine output less than 0.5 ml/kg/h for more than 6 hours Stage 2 - Injury SCr increased to more than 200% to 300% (2 to 3 times) from baseline Urine output less than 0.5 ml/kg per hour for more than 12 hours Stage 3 - Failure Increased to more than 300% (3 times) from baseline, or more than or equal to 4.0 mg/dl (X354 mmol/l) with an acute increase of at least 0.5 mg/dl (44 mmol/l) or on RRT Urine output less than 0.3 ml/kg/h for 24 hours or anuria for 12 hours AKIN Acute Kidney Injury Network Another valid diagnostic and staging tool Stage Serum Creatinine Urine Output 1 1.5-2 x baseline (or rise > 26.4 mmol/l) 2 >2-3 x baseline 3 > 3 x baseline (or > 354 mmol/l with acute rise > 44 mmol/l) < 0.5 ml/kg/hour for > 6 hours < 0.5 ml/kg/hour for > 12 hours < 0.3 ml/kg/hour for 24 hours or anuria for 12 hours PREVENTION 8

Focus on the preventable causes Key recommendations by KDIGO Guidelines Early detection monitoring of hemodynamic stability Volume expansion with isotonic crystalloids Vasopressors in the presence of vasomotor shock Avoid use of diuretics unless there is volume overload Insulin to control hyperglycemia Monitor aminoglycoside levels Discontinue other nephrotoxic drugs Monitor serum creatinine and urine output CLINICAL MANAGEMENT International AKI Management Guidelines Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int 2012; 2:1 138. 9

Management of AKI Secondary to Nephrotoxic Agents Monitor for elevated serum creatinine 1,2 Involve a clinical pharmacist to assist with medication management 2 Review medication list to identify nephrotoxic agents When more than one nephrotoxic drug is discontinue the drug most recent drug added. Consider replacing all other possible nephrotoxins with less toxic medications Provide supportive care: 1, 2 Monitor blood pressure Monitor intake and output Maintaining adequate hydration AKI resolves; follow-up in 3 months 2 1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical practice guideline for acute kidney injury. Kidney Int 2012; 2:1 138. 2. Vandenberghe, W., De Corte, W., Hoste, E.A.J. (2014). Contrast-associated AKI in the critically ill: relevant or irrelevant?. Current Opinion in Critical Care: 20(6):596-605. Continuous Renal Replacement Therapy Severe renal disease Utilizes a double lumen central venous catheter Indicated for patients who are hemodynamically instable for hemodialysis Mechanism CASE STUDIES 10